Apo E polvmorphism(e2, e3, e4) was among the first reported genetic polymorphism that explained part of the normal variation in plasma cholesterol concentrations. Both alleles E2 and E4 are significantly more frequent in patients with mixed forms of hyperlipidemia and contribute on the observed differences in CHD risk among different populations. Effects of apo E polymorphism on the distribution of plasma lipid profiles were studied in 105 normolipidemic healthy women. The relative frequencies of common alleles for gene locus of apo E in this study were that E3 allele was 0.848, E4 allele was 0.087, and E2 allele was 0.067. SBP and DBP were. slightly more elevated in E, allele than those in E3 and E4. The pulsation was also significantly(p <0.016) increased by E, allele with excess body fat % in E, allele. There were no differences in total-, total HDL-, VLDL+LDL-, VLDL- and LDL cholesterol among the apo E alleles. However, apo Ez allele subjects had lower levels of total HDL and HDL, cholestcrol(p <0.047) and significantly higher levels of HDL, cholesterol(p < 0.05) than those in apo E3 and E4 allele subject. The plasma TG levels were significantly higher in the apo E, allele than in the apo E3 allele, otherwise, the plasma TG level in E4 allele was significantly lower than that in E3 allele (p <0.049 among apo E alleles). Atherogenic indices(AI) such as (TC-HDL) / HDL(p X0.04) and HDL,,/ HDL2(p X0.06) were significantly increased in E2 allele than those in E3 and E4 allele. The conclusion is that first, it seems that apo E4-mediated alteration through L,DL B/E receptors or E receptors in cholesterol metabolism results in lower plasma TG or remnant particles and in higher levels of VLDL+LDL or LDL. Second, apo E, allele shows reciprocal effects of E4 on the plasma lipid metabolism, respectively. Third, apo E, allele was more atherogenic than apo E
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higher levels of HDL; / HDL, ratio and atherogenic index[(TC-HDL) / HDLI were criticized.
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